Conversely, if the entry of the SARS-COV-2 into the host cell requires the cleavage of the S protein into the S1 and S2 subunits by TMPRSS2 to promote pathogenicity and myocardial damage reported in COVID-19 patients [19, 20], we might speculate that DM vs. Non-DM might over-express these adverse clinical pathways. This evidence concerns the gene TMPRSS2 and COVID-19.